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Screening and Identification of Key Biomarkers in Clear Cell Renal Cell Carcinoma Based on Bioinformatics Analysis
bioRxiv preprint doi: https://doi.org/10.1101/2020.12.21.423889; this version posted December 23, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Screening and identification of key biomarkers in clear cell renal cell carcinoma based on bioinformatics analysis Basavaraj Vastrad1, Chanabasayya Vastrad*2 , Iranna Kotturshetti 1. Department of Biochemistry, Basaveshwar College of Pharmacy, Gadag, Karnataka 582103, India. 2. Biostatistics and Bioinformatics, Chanabasava Nilaya, Bharthinagar, Dharwad 580001, Karanataka, India. 3. Department of Ayurveda, Rajiv Gandhi Education Society`s Ayurvedic Medical College, Ron, Karnataka 562209, India. * Chanabasayya Vastrad [email protected] Ph: +919480073398 Chanabasava Nilaya, Bharthinagar, Dharwad 580001 , Karanataka, India bioRxiv preprint doi: https://doi.org/10.1101/2020.12.21.423889; this version posted December 23, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Abstract Clear cell renal cell carcinoma (ccRCC) is one of the most common types of malignancy of the urinary system. The pathogenesis and effective diagnosis of ccRCC have become popular topics for research in the previous decade. In the current study, an integrated bioinformatics analysis was performed to identify core genes associated in ccRCC. An expression dataset (GSE105261) was downloaded from the Gene Expression Omnibus database, and included 26 ccRCC and 9 normal kideny samples. Assessment of the microarray dataset led to the recognition of differentially expressed genes (DEGs), which was subsequently used for pathway and gene ontology (GO) enrichment analysis. -
Ovulation-Selective Genes: the Generation and Characterization of an Ovulatory-Selective Cdna Library
531 Ovulation-selective genes: the generation and characterization of an ovulatory-selective cDNA library A Hourvitz1,2*, E Gershon2*, J D Hennebold1, S Elizur2, E Maman2, C Brendle1, E Y Adashi1 and N Dekel2 1Division of Reproductive Sciences, Department of Obstetrics and Gynecology, University of Utah Health Sciences Center, Salt Lake City, Utah 84132, USA 2Department of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel (Requests for offprints should be addressed to N Dekel; Email: [email protected]) *(A Hourvitz and E Gershon contributed equally to this paper) (J D Hennebold is now at Division of Reproductive Sciences, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, Oregon 97006, USA) Abstract Ovulation-selective/specific genes, that is, genes prefer- (FAE-1) homolog, found to be localized to the inner entially or exclusively expressed during the ovulatory periantral granulosa and to the cumulus granulosa cells of process, have been the subject of growing interest. We antral follicles. The FAE-1 gene is a -ketoacyl-CoA report herein studies on the use of suppression subtractive synthase belonging to the fatty acid elongase (ELO) hybridization (SSH) to construct a ‘forward’ ovulation- family, which catalyzes the initial step of very long-chain selective/specific cDNA library. In toto, 485 clones were fatty acid synthesis. All in all, the present study accom- sequenced and analyzed for homology to known genes plished systematic identification of those hormonally with the basic local alignment tool (BLAST). Of those, regulated genes that are expressed in the ovary in an 252 were determined to be nonredundant. -
Mapping Influenza-Induced Posttranslational Modifications On
viruses Article Mapping Influenza-Induced Posttranslational Modifications on Histones from CD8+ T Cells Svetlana Rezinciuc 1, Zhixin Tian 2, Si Wu 2, Shawna Hengel 2, Ljiljana Pasa-Tolic 2 and Heather S. Smallwood 1,3,* 1 Department of Pediatrics, University of Tennessee Health Science Center, Memphis, TN 38163, USA; [email protected] 2 Environmental Molecular Sciences Laboratory, Pacific Northwest National Laboratory, Richland, WA 99354, USA; [email protected] (Z.T.); [email protected] (S.W.); [email protected] (S.H.); [email protected] (L.P.-T.) 3 Children’s Foundation Research Institute, Memphis, TN 38105, USA * Correspondence: [email protected]; Tel.: +1-(901)-448–3068 Academic Editor: Italo Tempera Received: 10 October 2020; Accepted: 2 December 2020; Published: 8 December 2020 Abstract: T cell function is determined by transcriptional networks that are regulated by epigenetic programming via posttranslational modifications (PTMs) to histone proteins and DNA. Bottom-up mass spectrometry (MS) can identify histone PTMs, whereas intact protein analysis by MS can detect species missed by bottom-up approaches. We used a novel approach of online two-dimensional liquid chromatography-tandem MS with high-resolution reversed-phase liquid chromatography (RPLC), alternating electron transfer dissociation (ETD) and collision-induced dissociation (CID) on precursor ions to maximize fragmentation of uniquely modified species. The first online RPLC separation sorted histone families, then RPLC or weak cation exchange hydrophilic interaction liquid chromatography (WCX-HILIC) separated species heavily clad in PTMs. Tentative identifications were assigned by matching proteoform masses to predicted theoretical masses that were verified with tandem MS. We used this innovative approach for histone-intact protein PTM mapping (HiPTMap) to identify and quantify proteoforms purified from CD8 T cells after in vivo influenza infection. -
CD40 Signaling Synergizes with TLR-2 in the BCR Independent Activation of Resting B Cells
CD40 Signaling Synergizes with TLR-2 in the BCR Independent Activation of Resting B Cells Shweta Jain, Sathi Babu Chodisetti, Javed N. Agrewala* Immunology Laboratory, Institute of Microbial Technology, Council of Scientific and Industrial Research, Chandigarh, India Abstract Conventionally, signaling through BCR initiates sequence of events necessary for activation and differentiation of B cells. We report an alternative approach, independent of BCR, for stimulating resting B (RB) cells, by involving TLR-2 and CD40 - molecules crucial for innate and adaptive immunity. CD40 triggering of TLR-2 stimulated RB cells significantly augments their activation, proliferation and differentiation. It also substantially ameliorates the calcium flux, antigen uptake capacity and ability of B cells to activate T cells. The survival of RB cells was improved and it increases the number of cells expressing activation induced deaminase (AID), signifying class switch recombination (CSR). Further, we also observed increased activation rate and decreased threshold period required for optimum stimulation of RB cells. These results corroborate well with microarray gene expression data. This study provides novel insights into coordination between the molecules of innate and adaptive immunity in activating B cells, in a BCR independent manner. This strategy can be exploited to design vaccines to bolster B cell activation and antigen presenting efficiency, leading to faster and better immune response. Citation: Jain S, Chodisetti SB, Agrewala JN (2011) CD40 Signaling Synergizes with TLR-2 in the BCR Independent Activation of Resting B Cells. PLoS ONE 6(6): e20651. doi:10.1371/journal.pone.0020651 Editor: Leonardo A. Sechi, Universita di Sassari, Italy Received April 14, 2011; Accepted May 6, 2011; Published June 2, 2011 Copyright: ß 2011 Jain et al. -
Supplement 1 Overview of Dystonia Genes
Supplement 1 Overview of genes that may cause dystonia in children and adolescents Gene (OMIM) Disease name/phenotype Mode of inheritance 1: (Formerly called) Primary dystonias (DYTs): TOR1A (605204) DYT1: Early-onset generalized AD primary torsion dystonia (PTD) TUBB4A (602662) DYT4: Whispering dystonia AD GCH1 (600225) DYT5: GTP-cyclohydrolase 1 AD deficiency THAP1 (609520) DYT6: Adolescent onset torsion AD dystonia, mixed type PNKD/MR1 (609023) DYT8: Paroxysmal non- AD kinesigenic dyskinesia SLC2A1 (138140) DYT9/18: Paroxysmal choreoathetosis with episodic AD ataxia and spasticity/GLUT1 deficiency syndrome-1 PRRT2 (614386) DYT10: Paroxysmal kinesigenic AD dyskinesia SGCE (604149) DYT11: Myoclonus-dystonia AD ATP1A3 (182350) DYT12: Rapid-onset dystonia AD parkinsonism PRKRA (603424) DYT16: Young-onset dystonia AR parkinsonism ANO3 (610110) DYT24: Primary focal dystonia AD GNAL (139312) DYT25: Primary torsion dystonia AD 2: Inborn errors of metabolism: GCDH (608801) Glutaric aciduria type 1 AR PCCA (232000) Propionic aciduria AR PCCB (232050) Propionic aciduria AR MUT (609058) Methylmalonic aciduria AR MMAA (607481) Cobalamin A deficiency AR MMAB (607568) Cobalamin B deficiency AR MMACHC (609831) Cobalamin C deficiency AR C2orf25 (611935) Cobalamin D deficiency AR MTRR (602568) Cobalamin E deficiency AR LMBRD1 (612625) Cobalamin F deficiency AR MTR (156570) Cobalamin G deficiency AR CBS (613381) Homocysteinuria AR PCBD (126090) Hyperphelaninemia variant D AR TH (191290) Tyrosine hydroxylase deficiency AR SPR (182125) Sepiaterine reductase -
An Overview of the Role of Hdacs in Cancer Immunotherapy
International Journal of Molecular Sciences Review Immunoepigenetics Combination Therapies: An Overview of the Role of HDACs in Cancer Immunotherapy Debarati Banik, Sara Moufarrij and Alejandro Villagra * Department of Biochemistry and Molecular Medicine, School of Medicine and Health Sciences, The George Washington University, 800 22nd St NW, Suite 8880, Washington, DC 20052, USA; [email protected] (D.B.); [email protected] (S.M.) * Correspondence: [email protected]; Tel.: +(202)-994-9547 Received: 22 March 2019; Accepted: 28 April 2019; Published: 7 May 2019 Abstract: Long-standing efforts to identify the multifaceted roles of histone deacetylase inhibitors (HDACis) have positioned these agents as promising drug candidates in combatting cancer, autoimmune, neurodegenerative, and infectious diseases. The same has also encouraged the evaluation of multiple HDACi candidates in preclinical studies in cancer and other diseases as well as the FDA-approval towards clinical use for specific agents. In this review, we have discussed how the efficacy of immunotherapy can be leveraged by combining it with HDACis. We have also included a brief overview of the classification of HDACis as well as their various roles in physiological and pathophysiological scenarios to target key cellular processes promoting the initiation, establishment, and progression of cancer. Given the critical role of the tumor microenvironment (TME) towards the outcome of anticancer therapies, we have also discussed the effect of HDACis on different components of the TME. We then have gradually progressed into examples of specific pan-HDACis, class I HDACi, and selective HDACis that either have been incorporated into clinical trials or show promising preclinical effects for future consideration. -
Exogenous Hydrogen Sulfide Plays an Important Role by Regulating
International Journal of Molecular Sciences Review Exogenous Hydrogen Sulfide Plays an Important Role by Regulating Autophagy in Diabetic-Related Diseases Shuangyu Lv , Huiyang Liu and Honggang Wang * Henan International Joint Laboratory of Nuclear Protein Regulation, School of Basic Medical Sciences, Henan University, Kaifeng 475000, China; [email protected] (S.L.); [email protected] (H.L.) * Correspondence: [email protected] Abstract: Autophagy is a vital cell mechanism which plays an important role in many physiological processes including clearing long-lived, accumulated and misfolded proteins, removing damaged organelles and regulating growth and aging. Autophagy also participates in a variety of biological functions, such as development, cell differentiation, resistance to pathogens and nutritional hunger. Recently, autophagy has been reported to be involved in diabetes, but the mechanism is not fully understood. Hydrogen sulfide (H2S) is a colorless, water-soluble, flammable gas with the typical odor of rotten eggs, which has been known as a highly toxic gas for many years. However, it has been reported recently that H2S, together with nitric oxide and carbon monoxide, is an important gas signal transduction molecule. H2S has been reported to play a protective role in many diabetes- related diseases, but the mechanism is not fully clear. Recent studies indicate that H2S plays an important role by regulating autophagy in many diseases including cancer, tissue fibrosis diseases and glycometabolic diseases; however, the related mechanism has not been fully studied. In this review, we summarize recent research on the role of H2S in regulating autophagy in diabetic-related diseases to provide references for future related research. -
Subcellular Distribution of HDAC1 in Neurotoxic Conditions Is Dependent on Serine Phosphorylation
The Journal of Neuroscience, August 2, 2017 • 37(31):7547–7559 • 7547 Neurobiology of Disease Subcellular Distribution of HDAC1 in Neurotoxic Conditions Is Dependent on Serine Phosphorylation Yunjiao Zhu,1* Oscar G. Vidaurre,1* XKadidia P. Adula,1 XNebojsa Kezunovic,1 XMaureen Wentling,1 X George W. Huntley,1 and XPatrizia Casaccia1,2 1Department of Neuroscience, Friedman Brain Institute, Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, New York 10029, and 2Advanced Science Research Center at the Graduate Center of the City University of New York, New York, New York 10031 Calcium-dependent nuclear export of histone deacetylase 1 (HDAC1) was shown previously to precede axonal damage in culture, but the in vivo relevance of these findings and the potential posttranslational modifications of HDAC1 remained elusive. Using acute hippocam- pal slices from mice of either sex with genetic conditional ablation of Hdac1 in CA1 hippocampal neurons (i.e., Camk2a-cre;Hdac1 fl/fl), we show significantly diminished axonal damage in response to neurotoxic stimuli. The protective effect of Hdac1 ablation was detected also in CA3 neurons in Grik4-cre;Hdac1 fl/f mice, which were more resistant to the excitotoxic damage induced by intraventricular injection of kainic acid. The amino acid residues modulating HDAC1 subcellular localization were identified by site-directed mutagenesis, which identified serine residues 421 and 423 as critical for its nuclear localization. The physiological phosphorylation of HDAC1 was decreased by neurotoxic stimuli, which stimulated the phosphatase enzymatic activity of calcineurin. Treatment of neurons with the calcineurin inhibitors FK506 or cyclosporin A resulted in nuclear accumulation of phospho-HDAC1 and was neuroprotective. -
Determining HDAC8 Substrate Specificity by Noah Ariel Wolfson A
Determining HDAC8 substrate specificity by Noah Ariel Wolfson A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy (Biological Chemistry) in the University of Michigan 2014 Doctoral Committee: Professor Carol A. Fierke, Chair Professor Robert S. Fuller Professor Anna K. Mapp Associate Professor Patrick J. O’Brien Associate Professor Raymond C. Trievel Dedication My thesis is dedicated to all my family, mentors, and friends who made getting to this point possible. ii Table of Contents Dedication ....................................................................................................................................... ii List of Figures .............................................................................................................................. viii List of Tables .................................................................................................................................. x List of Appendices ......................................................................................................................... xi Abstract ......................................................................................................................................... xii Chapter 1 HDAC8 substrates: Histones and beyond ...................................................................... 1 Overview ..................................................................................................................................... 1 HDAC introduction -
The Metabolic Regulator Histone Deacetylase 9 Contributes to Glucose Homeostasis
Page 1 of 53 Diabetes The metabolic regulator histone deacetylase 9 contributes to glucose homeostasis abnormality induced by hepatitis C virus infection Jizheng CHEN2, Ning WANG1, Mei DONG1, Min GUO2, Yang ZHAO3, Zhiyong ZHUO3, Chao ZHANG3, Xiumei CHI4, Yu PAN4, Jing JIANG4, Hong TANG2, Junqi NIU4, Dongliang YANG5, Zhong LI1, Xiao HAN1, Qian WANG1* and Xinwen Chen2 1 Jiangsu Province Key Lab of Human Functional Genomics, Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, 210029, China 2 State Key Lab of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430071, China 3 Key Laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, China 4 Department of Hepatology, The First Hospital of Jilin University, Changchun, 130021, China 5 Department of Infectious Diseases, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430074, China 1 Diabetes Publish Ahead of Print, published online September 29, 2015 Diabetes Page 2 of 53 *Correspondence: Qian WANG, Ph.D. Jiangsu Province Key Lab of Human Functional Genomics Department of Biochemistry and Molecular Biology Nanjing Medical University Nanjing 210029, China E-mail: [email protected] Fax: +86-25-8362 1065 Tel: +86-25-8686 2729 2 Page 3 of 53 Diabetes ABSTRACT Class IIa histone deacetylases (HDACs), such as HDAC4, HDAC5, and HDAC7 provide critical mechanisms for regulating glucose homeostasis. Here we report HDAC9, another class IIa HDAC, regulates hepatic gluconeogenesis via deacetylation of a Forkhead box O (FoxO) family transcription factor, FoxO1, together with HDAC3. Specifically, HDAC9 expression can be strongly induced upon hepatitis C virus (HCV) infection. -
Georgia's Newborn Screening Panel (Disorders)
Georgia’s Newborn Screening Panel (Disorders) Organic Acid Fatty Acid Oxidation Amino Acid Hemoglobinopathy Other • Beta Ketothiolase (BKT) • Caritine Uptake • Cobalamin A and B Defect Deficiency (Cbl A,B ) • Long Chain 3 • Glutaric Acidemia type hydroxyl acyl-CoA • Biotinidase I dehydrogenase • Argininosuccinic Deficiency • Congenital • 3OH 3-CH3 Glutaric Acidemia • Sickle Cell • Adrenal Aciduria (HMG) Medium Chain acyl- • Citrullinemia Disease Hyperplasia • Isovaleric Acidemia CoA dehydrogenase • Homocystinuria • Sickle SC Deficiency • Congenital (IVA) • Maple Syrup Urine Disease • Trifunctional Protein Hypothyroidism • 3 Methylcrotonyl-Co A Disease • Sickle Beta Deficiency • Cystic Fibrosis Carboxylase Deficiency • Phenylketonuria Thalassemia • Very Long chain • Galactosemia (3MCC) • Tyrosinemia • Multiple Carboxylase acyl-CoA Deficiency dehydrogenase Deficiency • Methylmalonic Acidemia (MMA) • Propionic Acidemia 3-methylcrotonyl-CoA carboxylase deficiency (3-MCC) (3-methel-crow-ton-eel co-A car-box-il-ace de-fish-in-sea) POSITIVE NEWBORN SCREEN What is a positive newborn screen? Newborn screening is done on tiny samples of blood taken from your baby’s heel 24 to 48 hours after birth. Newborn screening tests for rare, hidden disorders that may affect your baby’s health and development. The newborn screen suggests your baby might have a disorder called 3-MCC. There are many other conditions that can cause a similar positive result on newborn screening. A positive newborn screen does not mean your baby has 3-MCC or any of the other conditions above, but it does mean your baby needs more testing to know for sure. Your baby’s doctor will help arrange for more testing by specialists in disorders like 3-MCC. Sometimes, a baby has a positive newborn screen because the mother has a hidden form of 3-MCC. -
Transcriptional Analysis of Sodium Valproate in a Serotonergic Cell Line Reveals Gene Regulation Through Both HDAC Inhibition-Dependent and Independent Mechanisms
bioRxiv preprint doi: https://doi.org/10.1101/837732; this version posted November 12, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Transcriptional analysis of sodium valproate in a serotonergic cell line reveals gene regulation through both HDAC inhibition-dependent and independent mechanisms Priyanka Sinha1,2, Simone Cree1,2, Allison L. Miller1,2, John F. Pearson1,2,3, Martin A. Kennedy1,2. 1Gene Structure and Function Laboratory, Department of Pathology and Biomedical Science, University of Otago, Christchurch, New Zealand. 2Carney Centre for Pharmacogenomics, University of Otago, Christchurch, New Zealand. 3Biostatistics and Computational Biology Unit, University of Otago, Christchurch, New Zealand. Correspondence to: Prof. M. A. Kennedy Department of Pathology and Biomedical Science University of Otago, Christchurch Christchurch, New Zealand Email: [email protected] Keywords: RNA-Seq, NanoString, lithium, valproate, HDAC inhibitor, mood stabilizer 1 bioRxiv preprint doi: https://doi.org/10.1101/837732; this version posted November 12, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Abstract Sodium valproate (VPA) is a histone deacetylase (HDAC) inhibitor, widely prescribed in the treatment of bipolar disorder, and yet the precise modes of therapeutic action for this drug are not fully understood.